MicroRNAs (miRNAs) are small non-coding RNAs (~22 nucleotides in length), transcribed from non-protein coding genes or introns, which regulate gene expression through repressing translation and cleaving their mRNAs by binding to complementary sites in their 3'-untranslated region

Accumulating evidence has demonstrated that microRNAs (miRNAs) are involved in multiple processes in cancer development and progression. miR-326 has been identified as a tumor suppressor miRNA in several types of human cancer. However, the specific function of miR-326 and its target the nin one binding protein (NOB1) in colorectal carcinoma (CRC) remains unclear. In the present study, we found that miR-326 inhibited cell proliferation, migration and invasion, and induced cell apoptosis and cell cycle arrest of CRC cells by directly targeting NOB1. Furthermore, the upregulation of miR-326 in CRC cells was revealed to be associated with a feedback loop involving downregulation of the NOB1, which mimics the phenotype induced by miR-326. Importantly, we found that the CRC patients with high expression of miR-326 or low expression of NOB1 tend to obtain a better prognosis. Thus, for the first time, we provide convincing evidence that downregulation of miR-326 inhibited tumor proliferation and tumor metastasis by directly targeting NOB1 in CRC. NOB1 and miR-326 could be potential therapeutic targets for CRC. Introduction Colorectal carcinoma (CRC) is the third most frequently diagnosed malignancy and the third leading cause of mortality among cancer patients in the USA (1). Despite current therapeutic strategies combing adjuvant chemotherapy, surgery, radiotherapy and sometimes immunotherapy, the prognosis of CRC remains poor. The main reason for the current situation is that most CRC patients have distant metastasis at diagnosis or develop recurrent metastatic CRC following surgical treatment. Furthermore, lack of an accurate prognosis biomarker makes it difficult to predict the patients survival time after surgery. Although recent developments in molecular biology have provided insight into the molecular mechanisms of CRC, the fundamental molecular mechanisms underlying progression and metastasis in CRC have not been fully elucidated. Thus, identification of CRC metastasis-associated molecules may be beneficial for a further prediction of clinical outcomes and may ultimately be used to identify subsets of patients that may benefit from specific targeted therapies. MicroRNAs (miRNAs) are small non-coding RNAs (~22 nucleotides in length), transcribed from non-protein coding genes or introns, which regulate gene expression through repressing translation and cleaving their mRNAs by binding to complementary sites in their 3'-untranslated region (3'-UTR) (2). Currently, several aberrant expressed miRNAs have proven to be associated with carcinogenesis, tumor progression and metastasis in CRC and are taken as prognostic indicators for CRC including miR-150 (3), miR-28-5p/-3p (4), miR-200 (5), miR-494 (6) and many others. miR-326 was found downregulated and functioned as a tumor suppressor in multiple types of solid tumor and hematologic neoplasms, such as glioma (7,8), medulloblastoma (9), cholangiocarcinoma (10) and chronic lymphocytic leukemia (11). Yet, the clarification of the function and clinical significance of miR-326 in CRC are still at an early stage. The yeast nin one binding protein (NOB1) is an evolutionarily conserved protein (12) and is required for the biogenesis and function of 26s proteasome (13). It has been observed that genetic depletion of NOB1 suppresses the process of 20S pre-rRNA to mature 18S rRNA, producing markedly high levels of the 20S pre-RNA with novel degradation MicroRNA-326 functions as a tumor suppressor in colorectal cancer by targeting the nin one binding protein LEi WU1,2*, HUi HUi3*, Li-JUAN WANG4, HAO WANG1,2, QIU-FANg LIU2 and SU-XiA HAN1 1Department of Radiotherapy, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061; Centers of 2Radiotherapy and 3gynecological Oncology, Shaanxi Provincial Tumor Hospital, Xi'an, Shaanxi 710068; 4Department of Oncology, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China Received January 2, 2015; Accepted February 27, 2015 DOI: 10.3892/or.2015.3840 Correspondence to: Professor Su-Xia Han, Department of Radiotherapy, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi 710061,